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Fibromyalgia FIBROMYALGIA Leena Mathew, M.D. Director Pain Fellowship Associate Professor Department of Anesthesiology Columbia University disclosures I have no conflicts of interest objectives • Be able to accurately diagnose fibromyalgia • Understand the patho- mechanism of fibromyalgia • Identify a multimodal treatment plan for patients with fibromyalgia. prevalence / epidemiology Prevalence 2-8% 4 million fibromyalgia patients 9 1 : 2 1 $5945 annually per person 35-60 years old history classic criteria 1990 98% patients / 69% controls Sensitivity 88.4% specificity 81 1% fibromyalgia impact questionnaire ( FIQ) • validated 10-item instrument • sensitivity 93.1% / specificity 91.7% • Assesses impact on function and effect of treatment R. Bennett 2005 revised ACR 2010 criteria Eliminated tender point exam widespread pain Index 0-19 Symptom severity score 0-12 • Fatigue • Cognition • Un-refreshed sleep • Somatic symptoms WPI≥ 7 and SSS≥ 5 WPI= 3-6 and SSS≥ 9 Sensitivity 86%, specificity 90% revised 2011 ACR criteria Physician estimate of somatic symptoms eliminated and expanded the SSS 0-31 FM symptom scale (FS) 19 pain locations 6 self-reported symptoms- poor sleep, fatigue, poor cognition + headache, depression or abdominal pain FS ≥ 13 best meets criteria (sensitivity 96% and specificity 91%) 2016 revision • Generalized pain in 4 of 5 regions. • Symptoms > 3 months. • WPI ≥ 7 and SSS score ≥ 5 or WPI of 4–6 and SSS score ≥ 9. • Diagnosis of fibromyalgia valid irrespective of other diagnoses symptoms • Chronic widespread pain Anxiety 40% • Fatigue Depression 50% • Non restorative sleep Sleep 90% Fatigue 90% • Mood / cognitive Pain 100% disturbances. comorbidities Depression / anxiety Fatigue, cognitive ds Headache / migraines Allergies Temporomandibular ds Esophageal dysmotility IBS Low back pain Reactive airway Idiopathic paresthesias Pelvic pain, cystitis Adapted from Aaron LA et al , Arch Int Med 2000; 160:221-227 multidimensional pathology Inflammator Neurological Genetic Pain matrix y 1.Oxidative stress, 1, Aberrant transmission 1. 26% prevalence in 1° 1.Decreased binding of mitochondrial relatives vs. 19% in µ- receptors in r-ACC damage cause a 2 Serotonin/ NE and EAA unrelated subjects inflammatory state. 2. Volume change in 4. epidermal nerve fiber density 2. Multiple genetic amygdala, hippocampus, 2.Inflammatory polymorphisms effect PFC, ACC and insula. cytokines up- 5. CSF levels of SP and NG factor serotonin, NE dopaminergic regulated (IL10, and levels of serotonin, GABA, system expression 3.Abnormal central pain IL25, IL36A) NE. processing 3. Granulocyte-specific genes are down-regulated ( FCER1A, MS4A2, CPA3) abnormal pain processing normal Primary afferent NK-1 AMPA Pain neuron Release of EAA/ SP NMDA receptor Quiet glia fibromyalgia Primary afferent NK-1 Pain neuron AMPA Enhanced release EAA /SP NMDA receptor Activated glia Adapted from Bradley LA. Pathophysiology of Fibromyalgia. Am J Med 2009 genetic signature Genes Mechanism -X 8.5 risk in 1° relatives COMT Catecholamine metabolism -Differential RNA expression of ADRB2 (β2 adrenergic Altered sympathetic activity 421 genes identified in 70 receptor) patients and 70 controls HTR2A( serotonin Altered serotoninergic function receptor 2A) -Changes in gene expression and D4 polymorphism Altered dopaminergic function concentrations of microRNAs TAAR1 Modulates dopaminergic receptor -Expression signatures for fibromyalgia with 10 candidate CNR1 Cannabinoid receptor genes sensitivity 95% and RGS4 Protein G signaling specificity 96% Adapted from Ablin JN et al 2015 fMRI in fibromyalgia Comparison effects of similar pain intensity in patients and controls Arthritis & Rheumatism Volume 46, Issue 5, pages 1333-1343, 8 MAY 2002 DOI: 10.1002/art.1022 http://onlinelibrary.wiley.com/doi/10.1002/art.10225/full#fig2 fMRI in fibromyalgia Comparison effects of similar stimulus pressures in patients and controls Arthritis & Rheumatism Volume 46, Issue 5, pages 1333-1343, 8 MAY 2002 DOI: 10.1002/art.10225http://onlinelibrary.wiley.com/doi/10.1002/art.10225/full#fig3 environmental triggers • Infections (Epstein-Barr virus, Lyme disease, Q fever, hepatitis) • Physical trauma (motor vehicle collisions) • Psychological trauma ( deployment/ abuse/death / sexual ) therapeutic framework Education Collaboration Treatment Focus on progress interdisciplinary management Grade A evidence : • cognitive-behavioral therapy (CBT) • Aerobic exercise / PT • CAM therapies Opioids • EMG biofeedback / Neuro-feedback TPI BDZ Grade B evidence: • Pharmacotherapy Marijuan • Acceptance /commitment group therapy • Educational interventions a Grade C evidence: • Mindfulness FDA approved pharmacotherapy Pregablin Milnacipran Duloxetine Binds presynaptic calcium Inhibits NE reuptake Selective inhibition of channels decreases serotonin and NE reuptake glutamate, NE, SP 50 mg bid to 150 mg TID 12.5 mg QD to 50 mg BID 30 mg QD to 60 mg QD Meta-analysis-3 RCT n=1890 15-wk DBRCT n=1196 patients DBRCT n=588 patients reduces pain and improves 27-wk RCT n= 888 patients reduces pain severity and function Improves pain, fatigue and interference with quality of function. life summary • Fibromyalgia is a prototypical centralized pain syndrome • There is no agreed-upon FM phenotype or the exact mechanisms driving its multifactorial pathogenesis. • Both genetic and environmental triggers involved in development of fibromyalgia with changes in the pain matrix. • Management requires an interdisciplinary approach and collaboration. Be able to accurately diagnose fibromyalgia Understand the pathomechanism of fibromyalgia Identify a multimodal treatment plan for patients with fibromyalgia .
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